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E I Solntseva

Publications and source records attributed to E I Solntseva.

At least 19 recordsLinked to original sources
PubMed2001

The nootropic drug vinpocetine modulates different types of potassium currents in molluscan neurons.

Three types of high-threshold K+ currents were recorded in isolated neurons of the snail Helix pomatia using a two-microelectrode voltage clamp technique: transient K+ current (I(A)), delayed rectifier (I(KD)) and Ca2+-dependent K+ current (I(K(Ca))). Vinpocetine (1-100 microM) applied to the bath affected different types of K+ current in different ways: I(A) was increased (35+/-14%), I(KD) was moderately inhibited (20+/-9%) and I(K(Ca)) was strongly suppressed (45+/-15%). When I(A) and I(K(Ca)) were present in the same cell, vinpocetine exerted a dual effect on the total K+ current, depending on the amplitude of the test stimulus. In the presence of vinpocetine, the I-V curve crossed the control I-V curve. The inhibition of I(K(Ca)) by vinpocetine between 1 and 100 microM is unlikely to be a result of Ca2+ current (I(Ca)) suppression, as the latter was inhibited only at vinpocetine concentrations exceeding 300 microM. Dibutyryl cyclic GMP (dbcGMP) (but not dbcAMP) mimicked the effects of vinpocetine in the majority of cells tested (coefficient of correlation r=0.60, P<0.05, n=22). The data suggest that modulation of different types of K+ current in neuronal membrane can contribute, at least partially, to the nootropic effect of vinpocetine through the regulation of intracellular Ca2+ concentration.

Animals↗
PubMed2000

Enhancement of low-threshold A-current of the neuronal membrane by vinpocetine.

A low-threshold fast inactivating K+ current (I(Alth)) was recorded in isolated land snail neurons using the two-microelectrode voltage clamp method. A nootropic drug, vinpocetine, applied to the extracellular medium at a concentration of 1-100 microM potentiated I(Alth). The potentiation consisted in a rise of its peak amplitude and an increase of the half-decay time. Vinpocetine did not cause a shift of the steady-state activation and inactivation curves along the potential axis. Dibutyryl cyclic GMP (dcGMP) also increased the peak amplitude but did not change the time of current half-decay. dcAMP did not potentiate I(Alth). The possible role of K+-current potentiation in neuronal membranes in therapy of dementia is discussed.

Animals↗
PubMed1998

[Cyclic GMP mimicks potentiation effect of the nootropic agent vinpocetine on the high threshold A-current in the mollusk neurons].

High-threshold transient K+ current (IAht) was recorded using a two-microelectrode voltage clamp technique in isolated neurons of the land snail. Effect of the nootropic drug vinpocetine on this current was studied and compared with cyclic nucleotides. The drug either enhanced or left unaltered the IAht, and dibutyryl cyclic GMP (dcGMP) imitated the effect. These two effects were not additive. Dibutyryl cyclic AMP did not imitate, the vinpocetine effect and decreased the amplitude of the IAht. The findings suggest that the cGMP mediated the vinpocetine effect on the Iaht.

Animals↗
PubMed1997

The effects of piracetam and its novel peptide analogue GVS-111 on neuronal voltage-gated calcium and potassium channels.

1. With the use of the two-microelectrode voltage-clamp method, three types of voltage-activated ionic currents were examined in isolated neurons of the snail Helix pomatia: high-threshold Ca2+ current (ICa), high-threshold Ca(2+)-dependent K+ current (IK(Ca)) and high-threshold K+ current independent of Ca2+ (IK(V)). 2. The effect of bath application of the nootropics piracetam and a novel piracetam peptide analog, ethyl ester of N-phenyl-acetyl-L-prolyl-glycine (GVS-111), on these three types of voltage-activated ionic currents was studied. 3. In more than half of the tested cells, ICa was resistant to both piracetam and GVS-111. In the rest of the cells, ICa decreased 19 +/- 7% with 2 mM of piracetam and 39 +/- 14% with 2 microM of GVS-111. 4. IK(V) in almost all cells tested was resistant to piracetam at concentrations up to 2 mM. However, IK(V) in two-thirds of the cells was sensitive to GVS-111, being suppressed 49 +/- 18% with 1 microM GVS-111. 5. IK(Ca) appeared to be the most sensitive current of those studied to both piracetam and GVS-111. Piracetam at 1 mM and GVS-111 at 0.1 microM decreased the amplitude of IK(Ca) in most of the cells examined by 49 +/- 19% and 69 +/- 24%, respectively. 6. The results suggest that piracetam and GVS-111 suppression of voltage-activated calcium and potassium currents of the neuronal membrane may regulate (both up and down) Ca2+ influx into neurons.

Animals↗
PubMed1997

Ethanol decreases the tetraethylammonium-induced blockade of potassium channels in molluscan neurons.

A high threshold K+ current was recorded in isolated neurons of land snail using the two-microelectrode voltage clamp method. The K+ current consisted mainly of two components, the slow Ca(2+)-dependent K+ current (IK(Ca)) and a faster Ca(2+)-independent K+ current (IK(V)), the ratio of which varied from cell to cell. The action of ethanol on the blocking effects of K+ antagonists was studied. The following K+ antagonists were used: tetraethylammonium (TEA), 4-aminopyridine (4-AP) and quinine. Ethanol (2-200 mM) either produced no effect on the total K+ current or inhibited it by 6-20%. When applied in the presence of 4-AP or quinine, ethanol did not affect the blocking effect of these antagonists on K+ current, while the blocking effect of 0.1-5 mM TEA on both IK(Ca) and IK(V) rapidly (1-2 min) decreased after the application of 2-200 mM ethanol (n = 10/14). The modulating effect of ethanol was either transient or persistent in different cells. The effect persisted when the concentration of TEA was increased, thus suggesting a noncompetitive character of interaction between TEA and ethanol.

4-Aminopyridine↗
PubMed1995

Properties of slow early potassium current in neurons of snail Helix pomatia.

1. In isolated neurons of visceral ganglia of snail Helix pomatia a slow early outward current (IA) was studied using a two-microelectrode voltage clamp technique. 2. The time of activation and inactivation of IAS at -40 mV were 90-120 msec and 3-5 sec respectively. The removal of inactivation at -120 mV took 2-5 min. 3. The reversal potential of the IAS was about -80 mV in normal saline and was sensitive to the external potassium concentration, changing about 35 mV per fivefold change in potassium over the range from 4 to 20 mM. The results suggest that IA were due to K+. 4. The IA persisted in Ca2+ -free medium and in the presence of Ca2+ -channels blockers, e.g., Cd2+. 5. The IA were blocked by 1-10 microM extracellular 4-aminopyridine, 1 mM of tetraethylammonium ions, 1 mM of Ba2+, but one was resistant to 1 mM Cs+. 6. 4-aminopyridine had a dual effect on the IA. It blocked the normal current, and then appeared to increase the inactivated currents.

4-Aminopyridine↗
PubMed1993

[Frequency potentiation mechanisms of cyclic AMP-dependent responses of snail neurons].

Intracellular injection of cAMP with the help of microiontophoresis (5-40 nA, 1-10 s) into land snail neurons induces rapid membrane depolarization. Action potentials have not influence on the following cAMP-responses. When the intervals between cAMP-injections are less than 5 minutes the effect of frequency potentiation of cAMP-responses is obtained. The experiments with cAMP-injection from two different barrels of multibarreled microelectrode show that a change of the microelectrode barrels during repetitive injections causes an abolition of the frequency potentiation effect of cAMP-responses. The results suggest that the frequency potentiation effect of cAMP-responses may be explained by peculiarities of microiontophoresis.

Animals↗
PubMed1992

[Mechanisms of calcium current decay acceleration induced by cyclic AMP].

In isolated snail neurones the level of cyclic AMP was increased either by intracellular injection of cAMP or by extracellular application of dibutyryl-cAMP and the change of high-threshold calcium current (ICa) decay was investigated. In 20 from 38 neurones it was obtained that both fast and slow phases of ICa decay were accelerated 2-2.5 times as affected by cAMP. The effect did not depend on the test-pulse potential and was displayed on the IBa. In the double-pulse experiments it was shown that cAMP enhanced the influence of depolarized prepulses (Vc) on the ICa tested (It). Analysis of the It-Vc curve showed that cAMP enhanced both Ca(2+)-dependent and voltage-dependent inactivation of ICa. The experiments where the intervals between Vc and Vt varied have shown that cAMP slowed down the rate of Ca(2+)-channels recovery from inactivation. The results suggest that cAMP increases the affinity of the Ca(2+)-channel inactivating substrate for Ca(2+)-ions.

Animals↗
PubMed1991

[Enhancement of potential-dependent inactivation of calcium channels of mollusk neurons by tolbutamide].

A two-microelectrode voltage-clamp method was used to measure a potential-dependent Ca-current (ICa) on isolated snail neurons. Tolbutamide (1-5 mmol/l) and H-8 (1-30 mumol/l), inhibitors of kinase A, caused a decrease in the peak amplitude and an acceleration of the ICa decay during a depolarizing step. In the presence of tolbutamide a slow (tau 2) time constant of the ICa decay has grown 2-3 times stronger than fast (tau 1) time constant. Curves of inactivation obtained in double-pulse experiments have shown that after tolbutamide application an inactivation of the ICa enhanced when prepulses were to +30(-)+70 mV. The results suggest that dephosphorylation of Ca(2+)-channels enhances a potential-dependent component of the ICa inactivation.

Animals↗
PubMed1990

[The role of cAMP in generating mollusk neuron responses, related to negative slope conductance, to dopamine application].

Dopamine (DA)-induced steady-state inward current has been studied in isolated mollusc neurons through two different mechanisms: an increase in the slow potential-dependent Na(+)-conductance and a decrease in the K(+)-conductance. Dibutyryl-cAMP mimicked the both types of DA-responses. 3-Isobutyl-1-methylxanthine (IBMX) in low concentration potentiated DA-responses and in high concentration mimicked them. It was concluded that most of DA-induced inward current responses associated with a negative slope conductance are mediated by cAMP.

1-Methyl-3-isobutylxanthine↗
PubMed1990

[The mechanisms of the inhibiting action of cyclic adenosine monophosphate on the calcium current of intact mollusk neurons].

Experiments were conducted on isolated unidentified snail neurons using the method of voltage clamp by two-microelectrodes. The intracellular level of cAMP was increased either by intracellular injection of the cAMP or by extracellular application of dcAMP or isobutylmethylxanthine. The inhibitory effect of cAMP on the ICa was investigated as well as on the IBa. Intracellular injection of cGMP into the same neurons through multibarrel microelectrodes enhanced the ICa, while application of the phorbol ester had no effect on the ICa. Intracellular injection of EGTA enhanced the ICa, but the inhibitory effect of cAMP on the ICa was not changed in the presence of EGTA. Tolbutamide and H-8 (to the less degree) reduced the ICa. In 6 from 12 experiments the inhibitory effects of tolbutamide and dcAMP on ICa were not additive. The results suggest that the inhibitory effect of cAMP on the ICa is not due to the activation of cAMP- or cGMP-dependent protein kinase or protein kinase C. The cAMP effect does not depend on the cytoplasmic Ca2(+)-level. The possibility of the direct cAMP interaction with the Ca2(+)-channel is discussed.

Animals↗
PubMed1989

[Restoration of potential-dependent anti-brain antibody-inhibited calcium current by cyclic adenosine monophosphate].

A two-microelectrode voltage clamp method was used for measuring the voltage-dependent calcium current (ICa) in isolated nonidentified snail neurons. Intracellular injection of cyclic adenosine monophosphate (cAMP, 10nA, 5 min) and extracellular application of dibutyryl-cAMP (dcAMP, I mmol/l, 10-20 min) did not change the normal ICa or reversibly decreased the ICa amplitude by 10-20%. Extracellular application of antibodies against S-100 proteins resulted in a Ca2+-dependent inactivation of the ICa: the ICa amplitude dropped to 15 +/- 12% of its initial level; cAMP and dcAMP restored an amplitude of the inhibited ICa up to 50 +/- 11%. It is shown that the effect of cAMP on ICa of intact neurons depends on the cytoplasmic Ca2+-level.

Animals↗